The Molecular Biology of Compassion
Thousands of scientific studies have examined the possible genetic causes underlying brain/mind disorders such as schizophrenia, Alzheimer’s disease, depression, violence and criminality, and psychopathy. The more positive side of human behavior, with aspects such as altruism and empathy, has been studied much less – even though these are obviously much more valued from both transhumanist and typical humanist perspectives. Recently, however, this has begun to change, and these positive behaviors have been analyzed at the molecular level with interesting results.
The presence of clear molecular mechanisms underlying altruism and empathy is all the more interesting given the complex social, biological, evolutionary and chemical properties of these behaviors. Altruism consists of actions performed for the benefit of others, even at a loss to oneself, while empathy involves feeling sympathy for the suffering of others, often with a desire to help. Since the time of Aristotle, many scholars have noted the close association of altruism and empathy. It has long been thought that both are acquired from ones parents, with societal and religious influences also playing strong roles. However, clear examples of empathetic/altruistic behaviors are seen in many species ranging from bats to chimpanzees —; species which that do not appear to teach their offspring the rules of “being nice.” Also these behaviors are seen in children under eighteen 18 months, who are likely acting on innate behavior patterns and not onrather than parental teachings. Although it’s difficult to separate learned from genetically determined behaviors, studies of identical twins indicate that altruistic behaviors show a roughly ~40-50 percent% genetic heritability. Interestingly, one study demonstrated that religiousness positively correlated with altruistic behavior and negatively with anti-social behavior, although the magnitude of the correlations was modest at best.
Several evolutionary mechanisms have been proposed to explain empathy and altruism. These include kin selection, reciprocity, and group selection.; Aall of these are based on the idea that the altruistic individual will later receive benefits for altruistic actions. Additionally, several hormones and /neurotransmitters have been implicated in altruism and empathy. Oxytocin promotes affiliative behaviors, such as parental care and bonding, trust, empathy, the ability to infer the mental states of others, and reciprocity/generosity. Intranasal oxytocin administration increases generosity, while feelings of empathy are associated with a 47 percent% plasma oxytocin increase. Low oxytocin levels correlate strongly with a history of violence and suicide attempts. Other hormones/neurotransmitters have also been implicated in altruism/empathy, for example dopamine and serotonin activities enhance pro-social behaviors (generosity, altruism, and even moral behavior) and appear to alter and often increase oxytocin activity, while testosterone decreases generosity and genetic variations of its receptor are associated with criminal behavior.
While these theories and observations concerning hormone activities have some value in explaining the possible evolutionary and neurophysiological mechanisms underlying altruism/empathy, they do not explain its molecular-genetic basis or how the behaviors might be inherited. Recently molecular biology techniques have been used to analyze the neuromolecular factors that account for individual differences in social behavior. This new research area, termed “Social Neuroscience,”, has been applied to the analysis of altruism/empathy and gives insights into the well-known differences in individual propensity for these behaviors. Interestingly, many relatively large differences in altruistic and empathetic behaviors have been identified which come from one single base-pair difference in a gene sequence (called “single nucleotide polymorphisms or SNPs).
Analysis of normal variations of the oxytocin receptor DNA sequence has revealed many variations, many of which are SNPs. One analysis of this gene revealed sixteen SNPs, three of which correlated with increased altruism in the “Dictator Game” —- a game that involves donating money as a measure of altruistic behavior. One SNP, a thymine→guanine change towards the end of the oxytocin gene sequence, correlated in two independent sample populations with a 40 percent% increase in money donation. Interestingly, the same SNP also appears to play a role in individual risk for autism. The mechanism behind this one SNP altering altruistic behavior is not currently known, although it’s likely that the gene sequence change may increase oxytocin mRNA stability, resulting in more receptors and effectively stronger oxytocin hormonal signaling through these receptors.
Similarly, the arginine vasopressin receptor gene (AVPR1a) carries normally occurring DNA promoter (regulatory) gene region repeats that can be long or short. Individuals with the longer repeats showed significantly higher altruism in the Dictator Game than those with shorter repeats. In an unusual research protocol, the hippocampal regions of the research subject’s brains were analyzed shortly after their deaths. Individuals with the longer repeats showed higher brain hippocampal mRNA levels for the AVPR1a gene than those with the shorter repeat, suggesting that higher AVPR1a gene mRNA levels resulted in higher receptor protein levels, and higher AVPR1a gene product signaling, increasing altruistic behaviors.
In some studies, dopamine activity has been shown to increase oxytocin signaling and activity. Catechol-O-methyl transferase in an enzyme degrades dopamine in the area where two neural cells meet (the synaptic cleft), regulating neural signaling. One study found that one single DNA base change in the sequence coding for this enzyme accounted for 14.6 percent% of the variance seen in individual willingness to donate money to a child in a developing country, with individuals carrying one DNA base change donating twice as much money. Interestingly, the gene sequence change (guanine→adenine) caused a 3-4-three to fourfold reduction in enzyme activity, demonstrating that increased synaptic cleft dopamine (and therefore increased dopamine and oxytocin-signaling) increased altruistic behavior.
Lastly, testosterone and 5--dihydrotestosterone bind the androgen receptors and exert many different effects. Higher testosterone levels have been associated with increased male anger and aggression, risk-taking behaviors, and lowered fatigue and inertia, while increased aggression and violence have been associated with testosterone-related drug abuse. The androgen receptors normally carry three DNA base repeats (“triplets”), which show great variation among different individuals and populations. One study from India analyzed these repeats in the androgen receptor gene in 645 men,; 241 of whom were convicted for rape, 107 for murder, 26 for both crimes, and 271 “control males” who committed no crimes. The study showed a significant decrease in the triplet repeat number in men who committed crimes vs. those who did not (approximately ~17 vs. 21 repeats). Men who committed both crimes had the lowest number of triplet repeats. Interestingly, androgen receptor signaling increases with lower triplet repeat numbers, indicating that men with lower repeat numbers likely have increased testosterone-related signaling at the same testosterone hormone levels. Although there is far more to criminal behavior than testosterone levels and signaling, the study does demonstrate than a simple gene sequence variation can severely change the levels of empathy an individual might feel.
The few studies mentioned above are just a few of many that are beginning to reveal the molecular mechanisms underlying altruism/empathy. While the molecular mechanisms of how these genetic variations are poorly understood, several appear to increase the signaling of neurotransmitters associated with altruism/empathy, or in the case of the testosterone receptor, increase signaling that likely lowers altruism and empathy. Although this is a new area of research, with comparatively few studies, with over time a clearer picture of the molecular genetics of altruism/empathy will emerge, increasing our understanding of how specific neurotransmitters and gene sequences promote these behaviors and how they are inherited. Given time, epigenetic influences on altruism and empathy will probably also be identified. A “black box” remains of how specific neurotransmitter-initiated signaling alters neuronal function to eventually bring about changes in our consciousness with feeling of empathy, and concomitant altruistic and empathetic behaviors. Addressing this issue is an important challenge in molecular neuroscience.